Study on risk assessment of metals and metalloids used in high technology industry

本研究由两部分组成，一是半导体中使用的镓（Ga）、铟（In）和砷化合物的毒性评估，二是超导体中使用的钇(Y)和镧。Aoki和Fowler估计了半导体材料的肾毒性。在暴露于Ga、in和亚砷酸钠后，研究了大鼠肾近端上皮细胞原代培养物中蛋白质合成的变化。暴露于300 μ m GaCl_3或10 μ m亚砷酸盐下，7种蛋白质的合成受到显著刺激。300 μ m的InCl_3暴露对蛋白质合成无显著影响。300 μ m Ga和3 μ m亚砷酸对乳酸脱氢酶（LDH）的释放无显著影响。在没有明显细胞损伤的情况下，这些蛋白的诱导可能是暴露于Ga的早期指标。Fowler等人报道了接触砷对小鼠和大鼠妊娠和产前发育的影响。砷气体被认为是一种强效的溶血剂。然而，大气浓度的砷会导致母体脾脏增大，母体血液和胎儿肝脏中砷的可测量水平也不会对发育毒性的终点产生不利影响。平野和铃木研究了超导体材料对肺部的毒性作用。大鼠气管内灌注YCl_3。Y的肺清除率非常慢，半衰期估计为168天。透射电镜和x射线显微分析表明，Y定位于肺泡和间质巨噬细胞的溶酶体和基底膜。支气管肺泡灌洗液上清LDH活性的剂量效应对比显示，1 mol YCl_3相当于约1 / 3 mol镉化合物和约3 mol氧化锌的急性肺毒性效力。

This study consists of two Parts, which are i) toxicity assessment of gallium (Ga), Indium (In), and arsenic compounds used in semiconductor, and ii) yttrium (Y) and lanthanum used in superconductor.Aoki and Fowler estimated the renal toxicity of materials for semiconductors. Alterations in protein synthesis in primary cultures of rat kidney proximal epithelial cells were examined following exposure to Ga, In and sodium arsenite. Synthesis of seven proteins was markedly stimulated by exposure to 300 micro-M GaCl_3 or 10 micro-M arsenite. No significant changes in protein synthesis were observed with 300 micro-M InCl_3 exposure. Release of lactate dehydrogenese (LDH) from the cells was not significantly increase by exposure to concentration of 300 micro-M Ga and 3 micro-M arsenite or less. In the absence of overt cell injury, the induction of these proteins may be useful as an early indicator for exposure to Ga.Fowler at al. reported the effect of arsine exposure on pregnancy and prenatal development of mice and rats. Arsine gas was known to be a potent hemolytic agent. However, arsine at atmospheric concentrations that caused increases in maternal spleen size and measurable levels of arsenic in maternal blood and fetal livers did not adversely affect endpoints of developmental toxicity.Hirano and Suzuki examined the toxic effect of materials for superconductors on the lung. YCl_3 was instilled intratracheally into rats. Pulmonary clearance of Y was very slow and the halflife was estimated to be 168 days. Transmission electron microscopy and X-ray microanalysis suggested that Y was localized in lysosomes of alveolar and interstitial macrophages, and basement membranes. Comparative dose-effect profiles of LDH activity in bronchoalveolar lavage fluid supernatant revealed that 1 mol of YCl_3 is equivalent to about one-third mole of cadmium compounds and about 3 mol of zinc oxide in the potency for acute pulmonary toxicity.